Mouse-to-mouse allografts have confirmed the ability of both healthy glial progenitors and neural stem cells to out-compete deficient glial progenitors and myelinate hypomyelinated hosts (Lachapelle et al., 1994; Mitome et al., 2001; Yandava et al., 1999), providing some assurance as to the likely efficacy of human GPCs in myelinating myelin-deficient subjects, as in the hereditary leukodystrophies. But whether allografted GPCs can effectively compete with diseased or deficient GPCs in other disease settings is unclear. Such concerns are especially germane when considering the use of hGPC allografts in treating diffuse and multicentric disorders requiring whole neuraxis glial replacement, such as vanishing white matter disease in children, or chronic progressive multiple sclerosis in adults. Indeed, these questions will likely remain unanswered until human trials are performed, as there are limits to how effectively animal allografts can ever fully model the performance of human cells introduced into a human disease environment.
